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Anti-wrinkle by Anti-UV


What is wrinkle?

Beauty for men and women universally holds a boundless fascination. Societies throughout history have employed different forms of cosmetics and toiletries to improve appearance, scent and health. Cosmetic history takes us as far back as 3100 to 2907 BC; there is proof of naturally based and other types of make-up in Egypt. People of the Regency era used all sorts of berries, vegetables, herbs, flowers and other natural ingredients for makeup purposes.

Skin aging is usually associated with increased wrinkling, sagging and laxity. Wrinkles are one of the most natural and noticeable progressions of aging. While most of us would like to deter the changes occurring in our skin, unfortunately we cannot simply wish away the rate of aging. Wrinkles build up as a result of the slow wearing away of the epidermis (the outermost layer of skin) which is made up of dead tissue. When the cells in the deepest part of the epidermis known as the dermis die and become smaller, the skin loses its elasticity and resilience. As the tissue in the dermis shrinks, wrinkles are caused in the epidermis.

The mechanism of anti-wrinkle:

1, Inprove skin through improving cellular and molecular

2, Anti-oxidant

3, Anti-UV

4, Restore skin structure

In this E-Newsletter, we focus on how to keep our skin moisture with the fuction of Anti-UV.

Ultraviolet (UV) light is electromagnetic radiation with a shorter wavelength (<400 nm) than visible light, and consists mainly of UVA (315~400 nm), UVB (280~315 nm), and UVC (100~280 nm) bands. It is well established that UV induces various types of skin damage, such as DNA alterations, inflammation, oxidative alterations of collagen, melanin production, and skin cancer. UV-induced skin damage is considered to be caused, in part, by reactive oxygen species (ROS), such as singlet oxygen, generated in the skin by UV irradiation.

Ultravio let-A (UVA) light is particularly associated with oxidative processes involved in photoaging. A cascade of gene expression is initiated following UVA irradiation, which results in the upregulation of interstitial collagenase and the oxidative stress marker gene, heme-oxygenase I (HO-1). Singlet oxygen is strongly implicated as mediator in induction of these two genes. UVA penetrates deeper into the epidermis and dermis to a depth of approximately 1000 μm.

UVB is approximately 5% of total UVR and is predominantly responsible for a variety of skin diseases, including non-melanoma and melanoma skin cancers. It can penetrate the skin to a depth of approximately 160 ~180μm, crossing the epidermis layer and reaching the dermis.

UVC radiation is largely absorbed by the atmospheric ozone layer. However, it can penetrate the skin to a depth of approximately 60~ 80μm, is mutagenic and can damage DNA molecules.

Which products can be used for anti-wrinkle?

Vitamin E

The epidermis, acting as the primary barrier to fluid loss and environmental insult, is constantly exposed to UV light and other oxidative stressors. This constant oxidative barrage leaves its mark on the epidermis, resulting in phototoxicity, immunosuppression, photoaging, and cutaneous neoplasia. Because of its potent antioxidant and lipophilic properties, vitamin E is thought to play a key role in protecting epidermal cell membranes and lipids from oxidative damage. Numerous studies have demonstrated a role for topical vitamin E in reducing both acute and chronic UV-mediated skin responses, such as erythema and edema, sunburn-cell formation, DNA photo-adduct formation, immunesuppression, and photo-carcinogenesis. However, because of the inherent instability of α-Toc, both topical preparations and oral supplements often use inactive α-Toc esters (for example, α-tocopherol acetate). This may serve to increase shelf-life, but there is considerable debate as to whether appreciable bioconversion of these inactive esters to the active nonesterified form occurs in the skin. Moreover, there is some evidence that the use of these esterified tocopherols may actually enhance photo-carcinogenesis.

A novel hydrophilic γ-tocopherol derivative was recently synthesized to reinforce its biologic effects. γ-TDMG is superior to α-TA(α-Toc acetate) in blocking UVB induced photo-inflammation. In particular, the effectiveness of γ-TDMG in blocking UVB-induced photo-inflammation was maintained when it was applied after the UVB dose. This is important given the typical patterns of sunscreen use, in which sunscreen is applied just before or at some point after initial sun exposure. Given the ability of γ-TDMG to suppress PGE2 levels 1 hour after UVB irradiation, post treatment with γ-TDMG inhibits UVB-induced COX-2 activity, lipid peroxidation, reactive nitrogen oxide species formation, and inducible nitric oxide synthase suppression. Most importantly, γ-TDMG be a superior investigational tool for UVB photo-carcinogenesis studies.

Vitamin C

Vitamin C or L-ascorbic acid is an essential water-soluble substance known for its antioxidant properties and key role in collagen synthesis. Vitamin C has the ability to significantly improve abnormal skin pigmentation caused by chronic UV radiation exposure, including melasma. Vitamin C antioxidant properties contribute to its anti-aging effect as well, since ROS are known to interfere with fibroblasts and to destroy collagen and connective tissue structures.

The Raman spectra of DNA in different levels of vitamin C with 10- and 30-min ultraviolet (UV) radiations have be reported. The intensity of UV radiation was 18.68 W/m2. The experimental results proved that vitamin C could alone prevent UV radiation from damaging DNA, but the effects depended on the concentration of vitamin C. Vitamin C decreased UV radiation-induced DNA's damage. Maybe the reason is that when DNA in aqueous solution is radiated by UV, free radicals come into being, and vitamin C can scavenge free radicals, so vitamin C in lower concentration can protect DNA.

Raman spectra of damaged DNA can be obtained by using Raman spectra of the mixture of DNA and vitamin C subtracted relevant Raman spectra of vitamin C. Raman spectra of DNA in 0.15-mmol/L vitamin C with UV radiation were similar to that in 0.08-mmol/L vitamin C, but the fluorescence background noise of the latter was higher. Raman spectra of DNA in 0.45-mmol/L vitamin C with UV radiation were similar to that in 0.08-mmol/L vitamin C. Raman spectra of DNA in 1-mmol/L vitamin C with UV radiation had a very high fluorescence background noise, and any Raman characteristic bands could not be seen. There only some Raman spectra of damaged DNA are shown in Fig. 3 and 4. The band of 981 cm-1 which is corresponding to SO42- provides an internal intensity standard. All bands intensities were calculated by it.

Polyphenols in Red ginseng and Green tea

Red ginseng contains many bioactive constituents, including various ginsenosides and a polyphenol, panasenoside, that are believed to have antioxidant, immunostimulatory, and anti-aging activities. Polyphenol can decrease UV radiation-induced DNA's damage. UV-induced DNA damage in the form of cyclobutane pyrimidine dimers is considered as a molecular elicit for the induction of immunosuppression and initiation of photocarcinogenesis. Polyphenols, especially from green tea, scavenge H2O2 and inhibit UV induced oxidative DNA damage. Research has also revealed that an nucleotide excision repair mechanism is involved in the repair of photo-damaged DNA by green tea polyphenols, and that IL-12 has a role in this process. Sunscreen formulations containing 25% T. Sinensis (green tea) extract has been proved to protect against UV radiation-induced photoaging. A combination of topical as well as oral administration of tea extracts exhibits histological improvement in tissue elastic content. Green tea polyphenols catechin, epicatechin, epigallocatechin, epigallocatechin-3-gallate etc., were favorable sunscreen supplements for protecting the skin from the adverse effects of UV radiation-induced inflammation, oxidative stress and DNA damage. Catechin is able to significantly prolong lifespan and enhance resistance to oxidative and thermal stress.

Silybum marianum

Silibinin is a flavonolignan compound that is found abundantly in the extract of milk thistle plant (Silybum marianum). Topical or dietary administration of silibinin is found to strongly inhibit UVB-induced tumor initiation, promotion and complete carcinogenesis in SKH-1 hairless mouse skin. Silibinin protects from UVB-caused DNA damage in skin epidermal cells. Silibinin is also found in a number of high-end moisturizers to prevent cutaneous oxidative damage and photoaging.

Soy isoflavone

Daily intake of 40 mg soy isoflavone aglycones improves aged skin by increasing the skin elasticity. Genistein, an isoflavone, from soybeans substantially inhibits cutaneous aging induced by UV light in mice and photo-damage in humans. The mechanisms of action involve protection of oxidatively and photo-dynamically damaged DNA, down regulation of UVB-activated signal transduction cascades and antioxidant activities. Administration of a concentrated soy extract for 6 months exhibited improvements in skin health for postmenopausal women, mainly by increasing epithelium thickness, increasing concentrations of collagen and elastic fibers, and also the number of subcutaneous vessels.


AX (Astaxanthin) is a carotenoid found mainly in plants and marine seafood such as salmon, lobster, shrimp or crab and is well known to have antioxidant, anti-inflammatory and immunomodulatory activities. The major mode of action of AX is to scavenge ROS. Due to its scavenger potential for singlet oxygen (which is generated by UVA exposure), AX has been implicated in the marked inhibitory effects on UVA-induced oxidative cell damage. Thus, it is anticipated that the addition of AX to UVA-exposed fibroblasts in culture will prevent the UVA stimulated up-regulation of MMP-1. A redox imbalance has been shown to be closely linked to a variety of altered cellular responses in which the intracellular redox condition profoundly affects intracellular signaling pathways.

Post-treatment with AX, which has a potent capacity to scavenge singlet oxygen, results in the complete abrogation of UVA-enhanced mRNA levels of MMP-1, accompanied by the specific down-regulation of increased protein expression and activity of MMP-1. Further, AX has a weak inhibitory effect on UVA-enhanced levels of NEP mRNA in concert with the specific down-regulation of increased protein expression and activity of SFE/NEP. This is of particular relevance for understanding UVA-associated photo-aging in which an AX sensitive imbalance or loss of intracellular redox homeostasis is closely involved in the up-regulation of metalloprotease activity via MAP kinase signaling. AX can interfere with UVA-induced MMP-1 and SFE/NEP expression at concentrations as low as 4 mm suggest that topical or oral administration of AX might prevent UVA-associated photo-aging such as skin sagging or wrinkling.


Photodamaged skin exhibits wrinkles, pigmented spots, dryness and tumors. Solar UV radiation induces cyclobutane pyrimidine dimers (CPD) and further produces base oxidation by reactive oxygen species (ROS). ROS are thought to be a major factor to initiate the up-regulation of matrix metalloproteinases (MMPs) in keratinocytes and fibroblasts via activation of receptor proteins on the cell membrane of keratinocytes and fibroblasts, and to degrade fiber components in dermis, leading to wrinkle formation. Coenzyme Q10 (CoQ10) was reported to reduce ROS production and DNA damage triggered by UVA irradiation in human keratinocytes in vitro. Further, CoQ10 was shown to reduce UVA-induced MMPs in cultured human dermal fibroblasts. UVB radiation-induced cytokine production in keratinocytes may be inhibited by CoQ10, resulting in the reduction of MMPs in fibroblasts leading to wrinkle reduction. In vitro studies showed that UVB-induced IL-6 production of normal human keratinocyte (NHKC) decreased in the presence of CoQ10. Furthermore, MMP-1 production of fibroblasts cultured with the medium containing CoQ10 collected from UVB-irradiated NHKC significantly decreased during 24 h culture. In the clinical trial study, we found that the use of 1% CoQ10 cream for five months reduced wrinkle score grade observed by a dermatologist. Taken together, our results indicate that CoQ10 may inhibit the production of IL-6 which stimulate fibroblasts in dermis by paracrine manner to up-regulate MMPs production, and contribute to protecting dermal fiber components from degradation, leading to rejuvenation of wrinkled skin.

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